Development of new periodontal treatment based on the suppression of ostaoclast differentiation factor (ODE) on T cells and osteoblasts

基于抑制破骨细胞分化因子（ODE）对 T 细胞和成骨细胞的新型牙周治疗的开发

• 批准号: 14571977
• 负责人: NAGASAWA Toshiyuki
• 金额: $ 1.92万
• 依托单位: Tokyo Medical and Dental University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2002
• 资助国家: 日本
• 起止时间: 2002 至 2003
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-14571977/
• 关键词: osteoclast differentiation fact; OPG; RANKL; T cell; periodontitis; 歯周炎; プロスタグランジン; T細胞; ODF; 歯肉線維芽細胞; IL-1; PGE2

The purpose of the present study was to investigate the expression of osteoclast differentiation factor (ODE) and osteopmtegerin (OPG) in periodontitis, and develop a novel treatment to suppress the ODF in periodontitis. The results of the study were as follows;1) Human gingival fibroblasts express OPG, but they don't express ODE suggesting that human gingival fibroblasts suppress osteoclastogenesis.2) Human periodontal ligament cells expressed ODF in response to inflammatory stimulation, suggesting that inflammation extending to periodontal ligament might augment alveolar bone resorption.3) Human periodontal ligament cells produce bone morphogenetic protein (BMP) -2 in response to transforming growth factor beta(TGF-b).These results suggests that adequate amount of human gingival fibroblasts are needed to suppress osteoclastogenesis in periodontitis, arid it is important to evade the inflammation in near the periodontal ligament cells.

本研究旨在探讨破骨细胞分化因子（ODE）和骨调素（OPG）在牙周炎组织中的表达，并探讨抑制ODF的治疗方法。研究结果如下：1）人牙龈成纤维细胞表达OPG，但不表达ODE，表明人牙龈成纤维细胞抑制破骨细胞生成。2）人牙周膜细胞对炎症刺激有反应，表达ODF，提示炎症扩展到牙周膜可能会增加牙槽骨吸收。3）人牙周膜细胞产生骨形态发生蛋白（BMP）-结果提示，牙周炎时需要足够量的人牙龈成纤维细胞来抑制破骨细胞的生成，避免牙周膜附近细胞的炎症反应是重要的。

项目成果

Mahanonda R, Sa-Ard-Jan N, Yongvanitchit K, Wisetchang M, Ishikawa I, Nagasawa T, Waish DS, Pichyangkul S: "Up-regulation of co-stimulatory molecule expression and dendritic cell marker (CD83) on B cells in periodontal disease"J Periodont Res. 37. 177-183

Mahanonda R、Sa-Ard-Jan N、Yongvanitchit K、Wisetchang M、Ishikawa I、Nagasawa T、Waish DS、Pichyangkul S：“牙周 B 细胞上共刺激分子表达和树突状细胞标记物 (CD83) 的上调

Nagasawa T, Kobayashi H, Kiji M, Aramaki M, Mahanonda R, Kojima T, Murakarni Y, Saito M, Morotome Y, Ishikawa I: "LPS-stimulated human gingival fibroblasts inhibit the differentiation of monocytes into osteoclasts through the production of osteoprotegerin

Nagasawa T、Kobayashi H、Kiji M、Aramaki M、Mahanonda R、Kojima T、Murakarni Y、Saito M、Morotome Y、Ishikawa I：“LPS 刺激的人牙龈成纤维细胞通过产生骨保护素抑制单核细胞向破骨细胞的分化

Kobayashi H, Nagasawa T, Aramaki M, Noguchi K, Oda S, Ishikawa I: "Effect of genotype and expression intensity of Fc-gamma-receptor IIIb (CD16) on the severity of periodontitis in Japanese population"Dentistry in Japan. 40. 120-123 (2004)

Kobayashi H、Nagasawa T、Aramaki M、Noguchi K、Oda S、Ishikawa I：“Fc-γ-受体 IIIb (CD16) 基因型和表达强度对日本人群牙周炎严重程度的影响”日本牙科。

Iwasaki K, Noguchi KJshikawa I.: "Prostaglandin E2 downregulates interleukm-12 production through EP4 receptors in human monocytes stimulated with lipopolysaccharide fiom Actinobacillus"Oral Microbiol Immunol. 18. 150-155 (2003)

Iwasaki K、Noguchi KJshikawa I.：“前列腺素 E2 通过放线杆菌脂多糖刺激的人单核细胞中的 EP4 受体下调白细胞介素 12 的产生”口腔微生物免疫学。

長澤敏行, 石川 烈: "破骨細胞分化因子と破骨細胞形成抑制因子による歯槽骨吸収の調節"炎症と免疫. 12. 444-450 (2004)

Toshiyuki Nagasawa、Retsu Ishikawa：“破骨细胞分化因子和破骨细胞生成抑制因子对牙槽骨吸收的调节”炎症与免疫学 12. 444-450 (2004)。